ArticleJCI insight2019
Uncoupled turnover disrupts mitochondrial quality control in diabetic retinopathy.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma.bioRxiv : the preprint server for biology · 2026Article
- The Interaction Between Mitophagy Dysregulation and the Diabetic Bladder Microenvironment.Journal of diabetes · 2026Review
- Ginsenoside Rg1 ameliorates the senescence and neurite injury of retinal ganglion cells in DR via targeting VDR and promoting mitochondrial biogenesis.Journal of ginseng research · 2026Article
- The Central Role of Oxidative Stress in Diabetic Retinopathy: Advances in Pathogenesis, Diagnosis, and Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- FUNDC1-Associated Regulation of Mitochondrial Function Is Crucial for Preventing Endothelial Injury in Hyperglycemia.Oxidative medicine and cellular longevity · 2026Article
- Remodeling of the mitochondrial quality control network: natural products intervening in diabetic retinopathy.Frontiers in pharmacology · 2026Review
- Review
- Proliferative diabetic retinopathy subtypes defined by immune defense and endothelial mitochondrial dysfunction.Signal transduction and targeted therapy · 2025Article
- Exploiting autophagy and related pathways: pioneering new horizons in cataract therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Mitochondrial fission process 1 protein: a comprehensive review of its core roles in mitochondrial dynamics, disease, and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- A new perspective on protecting the blood-retinal barrier against injury in diabetic retinopathy: mitophagy.Frontiers in endocrinology · 2025Review
- Editorial: Physiological and pathological changes of the retina associated with ageing.Frontiers in cellular neuroscience · 2025Article
- Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024Review
- Dysfunctional Mitochondria Clearance in Situ: Mitophagy in Obesity and Diabetes-Associated Cardiometabolic Diseases.Diabetes & metabolism journal · 2024Review
- Classical and Innovative Evidence for Therapeutic Strategies in Retinal Dysfunctions.International journal of molecular sciences · 2024Review
- Relaxation of mitochondrial hyperfusion in the diabetic retina via N6-furfuryladenosine confers neuroprotection regardless of glycaemic status.Nature communications · 2024Article
- The sedoheptulose kinase CARKL controls T-cell cytokine outputs and migration by promoting metabolic reprogramming.Discovery immunology · 2024Article
- Impaired Removal of the Damaged Mitochondria in the Metabolic Memory Phenomenon Associated with Continued Progression of Diabetic Retinopathy.Molecular neurobiology · 2024Article
- m6A Modification-Association with Oxidative Stress and Implications on Eye Diseases.Antioxidants (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial quality control (MQC) is crucial for regulating CNS homeostasis, and its disruption has been implicated in the pathogenesis of some of the most common neurodegenerative diseases. In healthy tissues, the maintenance of MQC depends upon an exquisite balance between mitophagy (removal of damaged mitochondria by autophagy) and biogenesis (de novo synthesis of mitochondria). Here, we show that mitophagy is disrupted in diabetic retinopathy (DR) and decoupled from mitochondrial biogenesis during the progression of the disease. Diabetic retinas from human postmortem donors and experimental mice exhibit a net loss of mitochondrial contents during the early stages of the disease process. Using diabetic mitophagy-reporter mice (mitoQC-Ins2Akita) alongside pMitoTimer (a molecular clock to address mitochondrial age dynamics), we demonstrate that mitochondrial loss arose due to an inability of mitochondrial biogenesis to compensate for diabetes-exacerbated mitophagy. However, as diabetes duration increases, Pink1-dependent mitophagy deteriorates, leading to the build-up of mitochondria primed for degradation in DR. Impairment of mitophagy during prolonged diabetes is linked with the development of retinal senescence, a phenotype that blunted hyperglycemia-induced mitophagy in mitoQC primary Müller cells. Our findings suggest that normalizing mitochondrial turnover may preserve MQC and provide therapeutic options for the management of DR-associated complications.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.